SUMMARY: Increasing doses of alkylating agents such as -methyl--nitro--nitrosoguanidine, diethyl sulphate and ethylmethane sulphonate cause an inhibition of the expression of the and genes of wild-type This behaviour was not observed in a mutant which has a defective LexA repressor that is unable to bind to the SOS operator. Furthermore, an mutant showed the same behaviour as the wild-type strain indicating that the adaptive proteins are not responsible for the inhibition of and at high doses of alkylating agents. These results suggest that the inhibitory effect of these alkylating agents may be found in the interaction between the LexA repressor and the control regions of and On the other hand, high doses of either UV light or mitomycin C produced only a slight decrease in the induction of and , whereas bleomycin had no effect. The fact that a repressor structurally related to LexA repressor, such as LacI protein, showed the same behaviour as the LexA repressor when a Lac strain was treated with alkylating agents, suggests that these compounds can modify the binding abilities of repressors to DNA, producing a limited or even abolished release of repressors, and so decreasing the expression of inducible genes.


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